Abstract
Thromboxane A2 production in response to arachidonic acid and collagen in platelet rich plasma was studied in vitro. Maximal aggregation and T×A2 production was achieved at 4 ug/ml and 0.5 mM for collagen and arachidonic acid respectively. Hydralazine significantly inhibited T×A2 production in response to 4 ug/ml collagen independently of any inhibitory effect on platelet aggregation, and also inhibited both aggregation and T×A2 production in response to 0.5 mM arachidonic acid. Endralazine, a similar vasodilator was without effect. The inhibitory effect of hydralazine on T×A2 may be of value in the treatment of vascular disorders such as PIH.